别名 EBNA-1、EBNA1、EBV nuclear antigen 1 + [1] |
简介 Responsible for the origin of replication (oriP) dependent replication and maintenance of viral episomes during latent infection (PubMed:2996781, PubMed:15479791). EBNA1 dimer interacts with the DS (dyad symmetry) element within the origin of replication oriP and with a host mitotic chromosome to initiate viral DNA replication during latency (PubMed:2996781, PubMed:8551585, PubMed:24067969, PubMed:31142669). EBNA1 binding to DS recruits the host origin recognition complex (ORC) (PubMed:12953058). Governs the faithful mitotic segregation of the viral episomes by binding both the FR (family of repeats) element within oriP and the host mitotic chromosomes (PubMed:15479791, PubMed:11172042, PubMed:24067969). Forms a cell cycle-dependent tyrosine-dependent DNA cross-link and single-strand cleavage at oriP required for terminating replication and maintaining viral episomes (PubMed:33482082). Counteracts the stabilization of host p53/TP53 by host USP7, thereby decreasing apoptosis and increasing host cell survival (PubMed:15808506). Induces degradation of host PML through the ubiquitin-proteasome system, which promotes lytic reactivation and may impair the host cell DNA repair (PubMed:18833293). Increases the association of CK2 with PML proteins which increases the phosphorylation of PML proteins by CK2, triggering the polyubiquitylation and degradation of PML (PubMed:20719947). Displays inhibitory effects on a SUMO2-modified complex that includes STUB1, KAP1 and USP7 (PubMed:32176739). This inhibitory effect possibly participates to the maintenance of latency linked to PML silencing (PubMed:32176739). |
靶点 |
作用机制 EBNA1抑制剂 |
在研适应症 |
非在研适应症 |
最高研发阶段临床2期 |
首次获批国家/地区- |
首次获批日期1800-01-20 |
靶点 |
作用机制 EBNA1抑制剂 |
在研机构 |
原研机构 |
在研适应症 |
非在研适应症- |
最高研发阶段临床前 |
首次获批国家/地区- |
首次获批日期1800-01-20 |
作用机制 EBNA1调节剂 [+2] |
在研机构- |
在研适应症- |
最高研发阶段无进展 |
首次获批国家/地区- |
首次获批日期1800-01-20 |
开始日期2022-01-25 |
申办/合作机构 Stanford University [+2] |
开始日期2019-12-27 |
申办/合作机构 |
开始日期2019-04-04 |
申办/合作机构 |